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Pesticides -> Organochlorine Pesticides

Organochlorine pesticide

Pesticide

log Kow = 6.91

6.91

6.36

5.1

Odorless or with slight aromatic odor

It possesses fruit-like odor

... Slight, aromatic odor.

1.56 at 59 °F (USCG, 1999) - Denser than water; will sink

0.98 to 0.99

1.6 g/cm³

0.98-0.99 @25 °C

0.99

Biaxial elongated tablets, needles from 95% alcohol

Chemically pure p,p-DDT consists of white needles

Colorless crystals or off-white powder ...

less than 1 mg/mL at 70 °F (NTP, 1992)

Soluble in acetone, ether, benzene, carbon tetrachloride, kerosene, dioxane, and pyridine.

High solubility in fat (100,000 ppm)

Solubility, g/100 mL solvent: 58 acetone; 78 benzene; 42 benzyl benzoate; 45 carbon tetrachloride; 74 chlorobenzene; 116 cyclohexanone; 2 g/100 ml 95% alcohol; 28 ethyl ether; 10 gasoline; 3 isopropanol; 8-10 kerosene; 75 morpholine; 11 peanut oil; 10-16 pine oil; 61 tetralin; 50 tributyl phosphate.

Practically insoluble in dilute acids, alkalies. ... Freely soluble in pyridine, dioxane; solubility in organic solvents increases with rise in temperatures.

For more Solubility (Complete) data for DDT (8 total), please visit the HSDB record page.

324 to 340 °F (NTP, 1992)

162-171 °F (closed cup)

75 °C (closed cup)

162-171 °F

500 °F at 760 mmHg (NTP, 1992)

260 °C; 186 °C at 0.05 mm Hg

260 °C

260 °C @760 [mm Hg]

230 °F (Decomposes)

Danger

H301: Toxic if swallowed [Danger Acute toxicity, oral]

P203, P260, P264, P270, P273, P280, P301+P316, P318, P319, P321, P330, P391, P405, and P501 (click each P-code to see the statement)

Danger

H301+H311 (38%): Toxic if swallowed or in contact with skin [Danger Acute toxicity, oral; acute toxicity, dermal]

P203, P260, P262, P264, P270, P273, P280, P301+P316, P302+P352, P316, P318, P319, P321, P330, P361+P364, P391, P405, and P501 (click each P-code to see the statement)

Hazard Traits - Bioaccumulation; Carcinogenicity; Developmental Toxicity; Endocrine Toxicity; Environmental Persistence; Hepatotoxicity and Digestive System Toxicity; Neurotoxicity; Reproductive Toxicity

Regulation (EC) No 178/2002 (amended)

S - indicates a substance that is identified in a final Significant New Use Rule.

Substance: Clofenotane

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

Special Hazards of Combustion Products: Toxic and irritating gases may be generated

Combustible. Liquid formulations containing organic solvents may be flammable. Gives off irritating or toxic fumes (or gases) in a fire.

Behavior in fire: Melts and burns.

Material itself does not burn or burns with difficulty /Organochlorine pesticides, solid, toxic/.

Contact with strong oxidizers may cause fire and explosion hazard.

Very large doses are followed promptly by vomiting, due to local gastric irritation; delayed emesis or diarrhea may occur. With smaller doses, symptoms usually appear 2-3 hours after ingestion. These include tingling of lips, tongue, and face; malaise, headache, sore throat, fatigue, coarse tremors of neck, head, and eyelids; apprehension, ataxia, and confusion. Convulsions may alternate with periods of coma and partial paralysis. Vital signs are essentially normal, but in severe poisoning the pulse may be irregular and abnormally slow; ventricular fibrillation and sudden death may occur at any time during acute phase. Pulmonary edema usually indicates solvent intoxication. (USCG, 1999)

Still used in some parts of the world, DDT persists in the environment and in animal tissues. It has been especially harmful to predator species of birds. High-dose animal studies show that organochlorine insecticides are toxic to the liver. [LaDou, p. 553] Allergic contact dermatitis reported in farmworkers; [Kanerva, p. 1777] Despite the billions of pounds of DDT that have been manufactured and used, hepatic injury acquired as the result of occupational or environmental exposure to it remains to be reported. [Zimmerman, p. 413]

The major hazards encountered in the use and handling of DDT stem from its toxicologic properties as an organochlorine pesticide. While DDT may exert toxic effects from all routes of exposure, acute effects from ingestion are the most dramatic and frequently experienced, ranging from vomiting and diarrhea to coarse tremors, convulsions, and death. Effects from dermal contact (eg, dermatitis) and inhalation (eg, irritation of the nose and throat) have been noted, but are rare. To protect against its toxic effects in areas where there may be detectable amounts of DDT (eg, formulation and application activities) workers should wear protective clothing (including neoprene gloves and apron), and a self-contained or supplied-air respirator with a full facepiece and operated in positive-pressure mode. While OSHA established a PEL of only 1 mg/cu m as an 8 hr TWA in workplace air, it is still recommended that strict adherence to personal hygiene be maintained, including the daily cleaning of protective equipment and clothing, and washing of exposed skin with soap and water before eating and at the end of the work day. DDT will not ignite easily (flashpoint 162-171 °F closed cup), but it will burn with the potential of giving off irritating or poisonous gases. For small fires involving DDT, extinguish with dry chemical, CO2, water spray, or foam, and for large fires, use water spray, fog, or foam. Runoff from fire control water may give off poisonous gases or cause water pollution and should therefore, be controlled (eg, diked for later disposal). DDT may be stored in bottles, tins, bags, or fiber drums, but not in iron drums. DDT is reactive with iron and aluminum salts, as well as alkaline substances. Shipping containers should bear the label, "Keep Away From Food". Spills of DDT should be quickly contained. Small spills (liquid DDT first absorbed by non-combustible material, eg, sand) are carefully shovelled into a container for later disposal. Large land spills are diked or deposited in excavated pits, ponds, or other holding areas (dry spills are covered with plastic sheet) for later disposal. Large spills on water first may need to be trapped at the bottom with sand bag barriers or treated by an application of activated charcoal, then removed by suction hose or mechanical dredge. Before permanent land disposal of DDT, consult with environmental regulatory agencies. In addition to land disposal, a variety of incineration techniques have been successful in destroying DDT with over a 99% efficiency.

European Commission, ESIS; IUCLID Dataset, Clofenotane (50-29-3) (2000 CD-ROM edition).[Available from, as of June 5, 2009: http://esis.jrc.ec.europa.eu/]

WHO; Environ Health Criteria: DDT and its Derivatives (1979). These monographs are designed for scientists and administrators responsible for the establishment of safety standards and regulations and provide basic scientific risk evaluations of a wide range of chemicals and groups of chemicals.

USEPA; Ambient Water Quality Criteria Doc: DDT (1980) EPA 440/5-80-038

USEPA; DDT. A Review of Scientific and Economic Aspects of Decision to Ban its Use as a Pesticide. (1975) EPA 520/1-75-022

For more Special Reports (Complete) data for DDT (12 total), please visit the HSDB record page.

Fire Extinguishing Agents: Water, foam, dry chemical, or carbon dioxide (USCG, 1999)

Use water spray, powder, foam, carbon dioxide.

Fresh air, rest.

Remove contaminated clothes. Rinse and then wash skin with water and soap.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Give a slurry of activated charcoal in water to drink. Rest. Refer for medical attention .

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

(General first aid procedures)

TIH (Toxic Inhalation Hazard) - Term used to describe gases and volatile liquids that are toxic when inhaled. Some are TIH materials themselves, e.g., chlorine, and some release TIH gases when spilled in water, e.g., chlorosilanes. [ERG 2016].

1.0 [mg/m3], inhalable fraction[German Research Foundation (DFG)]

Fire extinguishing agents: Water, foam, dry chemical, or carbon dioxide.

Extinguish fire using agent suitable for type of surrounding fire. /Organochlorine pesticides, solid, toxic/

Do not extinguish fire unless flow can be stopped. Use water in flowing quantities as fog. Solid streams of water may be ineffective. Cool off all affected containers with flooding quantities of water. Apply water from as far a distance as possible ... /Organochlorine pesticide, liquid, flammable, toxic; Organochlorine pesticides, liquid, toxic; Organochlorine pesticides, liquid, toxic, flammable/

... Should not be kept in iron containers and should not be mixed with iron and aluminum salts nor with alkaline substances. High storage temperatures should also be avoided.

PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practicable to lab in which carcinogens are to be used, so that only small quantities required for ... expt need to be carried. Carcinogens should be kept in only one section of cupboard, an explosion-proof refrigerator or freezer (depending on chemicophysical properties ...) that bears appropriate label. An inventory ... should be kept, showing quantity of carcinogen & date it was acquired ... Facilities for dispensing ... should be contiguous to storage area. /Chemical Carcinogens/

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a POTW is acceptable only after review by the governing authority. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must meet Hazardous Material Criteria for disposal.

Land spill: Dig a pit, pond, lagoon, or holding area to contain liquid or solid material. Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash, cement powder, or commercial sorbents. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with a impermeable flexible membrane liner./

Water spill: Use natural deep water pockets, excavated lagoons, or sand bag barriers to trap material at bottom. If dissolved, apply activated carbon at ten times the spilled amount in region of 10 ppm or greater concentration. Remove trapped material with suction hoses. Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates.

The applicability of carbon to remove toxicants on EPA's published list and fish kill due to influent and effluent from five industrial plants currently using adsorption as a treatment method are examined. In the laboratory, activated carbon can achieve levels of less than 1 mg/L of aldrin, dieldrin, endrin, 1,1-dichloro-2,2-bis(p-chlorophenyl)ethene, 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane, 1,1-dichloro-2,2-bis(p-chlorophenyl)ethane, toxaphene, and Aroclor 1254. In operating plants, the toxicity of wastes to fish due to unknown constituents is significantly reduced or totally removed by activated carbon treatment.

For more Cleanup Methods (Complete) data for DDT (6 total), please visit the HSDB record page.

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number U061, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

DDT is a potential candidate for incineration by rotary kiln with a temperature range of 820 to 1600 °C and residence time of seconds for liquids and gases, and hours for solids.

Group I Containers: Combustible containers from organic or metallo-organic pesticides (except organic mercury, lead, cadmium, or arsenic compounds) should be disposed of in pesticide incinerators or in specified landfill sites. /Organic or metallo-organic pesticides/

Group II Containers: Non-combustible containers from organic or metallo-organic pesticides (except organic mercury, lead, cadmium, or arsenic compounds) must first be triple-rinsed. Containers that are in good condition may be returned to the manufacturer or formulator of the pesticide product, or to a drum reconditioner for reuse with the same type of pesticide product, if such reuse is legal under Department of Transportation regulations (eg 49 CFR 173.28). Containers that are not to be reused should be punctured ... and transported to a scrap metal facility for recycling, disposal, or burial in a designated landfill. /Organic or metallo-organic pesticides/

For more Disposal Methods (Complete) data for DDT (20 total), please visit the HSDB record page.

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Sweep spilled substance into covered sealable, non-metallic containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. Quality assurance to ascertain the completeness of the cleaning procedures should be implemented before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at end of shift, but should remain at employee's place of work for cleaning.

To avoid undue exposure of householders and spray operators to DDT, standard operating procedures and national guidelines should be in place and strictly followed. Appropriate management of DDT also entails adoption and enforcement of stringent rules and regulations to avoid leakage (into e.g. agriculture) and misuse (when used in, e.g., domestic hygiene). This includes the possibility of appropriate legal measures in the event that individuals or entities do not comply with this condition.

... Workers employed on formulating and application of DDT should be subject to precautionary measures, ... provided with suitable work clothing and ... protective equipment. Adequate sanitary facilities, including showers should be provided and need for personal hygiene stressed.

For more Preventive Measures (Complete) data for DDT (20 total), please visit the HSDB record page.

DDT was detected in all 55 samples of biopsy adipose tissues taken from male and female subjects in Punjab, India at a mean concn of 6.86 mg/kg. Maximum concns were observed in subjects 50 years and older(1). In blood samples taken from 18 male volunteers from the urban area of Ahmedabad, India, DDT was detected in 17 of the samples at a mean concn of 9.28 ug/L with a range of 3.66 - 24.06 ug/L(2). DDT was detected in the breast milk of 30 volunteers in Chiang Mai Province, Thailand at a mean concn of 10.3 ng/mL, a maximum of 38.2 ng/mL, and a detection frequency of 77%(3). The breast milk of 87 mothers in Tunisia were analyzed throughout their lactation periods. A mean DDT concn of 1.015 mg/kg fat weight, a range of 0.029 - 8.442 mg/kg, and a frequency of 88.5% were reported(4). Samples of breast milk were analyzed for pesticide levels from the 68 mothers of healthy boys (control) and 62 mothers of boys with cryptorchidism. DDT was detected in all samples with a mean concn of 4.63 ng/g lipid (range = 1.85 to 14.26 ng/g lipid) from volunteers who had sons with cryptorchidism and 3.98 ng/g lipid (range = 1.46 to 37.88 ng/g lipid) from volunteers with healthy children(5).

DDT was detected in human breast milk extracts collected from 54 samples in the United Kingdom at a mean concn of 6.2 ng/g lipid, a range of 1.1 to 760 ng/g lipid, and a frequency of 100%(1). Milk and prenatal blood samples obtained from Japanese women had reported DDT levels of 14.4 ng/g lipid (n = 125) and 15.0 ng/g lipid (n = 50), respectively(2). DDT was detected in human milk samples of 300 women (mean age = 23.1 years) residing in the area of Veracruz, Mexico taken between August 1996 and March 1997. The mean DDT concn was reported as 2.141 mg/kg fat basis, with a mean of 0.500 mg/kg for those residing in the urban area, 3.006 mg/kg in the suburban area, and 1.957 mg/kg in the rural area. Estimated daily intake of DDT and metabolites were reported as 14.437 mg/kg body weight/day (urban), 58.582 mg/kg body weight/day (suburban), and 43.318 mg/kg body weight/day (rural)(3). The blood of 120 Swedish male volunteers had reported total DDT (p,p'DDT, p,p-DDD, p,p-DDE) concns of 834 ng/g fat(4).

DDT was detected in 102 of 102 samples of human milk in 1979-1980 from the US at an avg concn of 0.19 ppm(1). DDT was detected in human milk from Canada, Finland and the Netherlands at concns of 3.8-5.5 ppb(2), 1.2 ppb (avg)(3) and 0.1-3.3 ppb(4), respectively. DDT was detected in 99 out of 99 human fat tissues sampled in Canada in 1976 at concns of 0.016-3.99 ppm(5). p,p'-DDT was detected in human fat tissue in the UK at mean concns of 1.2 ppm (males), and 1 ppm (females) for 1963-1964; 0.83 ppm (males), and 0.68 ppm (females) for 1965-1967; 0.54 ppm (males), and 0.49 ppm (females) for 1969-1971; 0.20 ppm (males), and 0.23 ppm (females) for 1976-1977(6). p,p'-DDT was detected in blood samples from Canadian females 7-98 days after giving birth at concns of 0.05-0.30 ppb(2). p,p'-DDT was detected in females in Zagreb, Yugoslavia (1978-1981) at an avg concn of 8.1 ppb and in children at an avg concn of 3.2 ppb(7). DDT was detected in the plasma lipids of fisherman around the St. Lawrence River at concns of 0.01-3.41 ug/g in 1995(8,9). DDT was detected in the blood of female residents of Veracruz, Mexico at concns of 0.7-212.3 ng/L(10). DDT was detected in human milk fat samples from Mexico at concns of 0.24-1.98 ug/g and in human adipose tissue from Mexico at concns of 0.48-1.08 ug/g(11).

... In rat, combined administration of DDT and aldrin leads to increased excretion of dieldrin. In beagles, repeated administration of DDT plus aldrin resulted in markedly augmented retention of DDT in blood and body fat. Pretreatment of rats & sheep with DDT has been shown to potentiate hepatotoxicity of carbon tetrachloride.

DDT, inducer of cytochrome P450-dependent monooxygenases, protects mice against acute toxic effects of parathion.

... DDT ... was found to induce microsomal enzymes and thus reduce the carcinogenicity of azo dyes and similar carcinogens. ... A major element for the reduced carcinogenicity is the increased detoxification through conjugation reactions with formations of glucuronides, sulfates, or glutathione conjugates. ... If DDT administration is not at the same time as a carcinogen, but subsequently, the ... decrease /in/ carcinogenic effect /disappears/. ... The mechanism ... may depend on an increased duplication of transformed cells.

... The toxicity of chloroform can be enhanced by the addition of a microsomal stimulator such as DDT to the diet.

For more Interactions (Complete) data for DDT (8 total), please visit the HSDB record page.

Exposure to DDT causes loss of weight and anorexia. DDT poisoning affects CNS function in humans, but pathologic changes are observed in the liver and reproductive organs. Hypertrophy of hepatocytes and subcellular organelles such as mitochondria, proliferation of smooth endoplasmic reticulum, centrolobular necrosis after exposure to high concentrations, and an increase in the incidence of hepatic tumors have been noted. (T10)

LC50; Species: Colinus virginianus (Bobwhite quail, 2 weeks old) oral ad libitum 611 ppm for 5 days (95% confidence limit: 514-724 ppm)

LC50; Species: Colinus virginianus (Northern bobwhite, subadult, weight 202.4 g (181-228 g)) dietary (incorporated into food; ad libitum) 1610 ppm for 5 days (1331-1948 ppm)

LC50; Species: Colinus virginianus (Northern bobwhite, subadult, weight 143.8 g (126-158 g)) dietary (incorporated into food; ad libitum) 1170 ppm for 5 days (830-1650 ppm)

LD50; Species: Coturnix japonica (Japanese quail, male 2 months old) oral 841 mg/kg (95% confidence limit 607-1170 mg/kg) /Purity 77.2%/

For more Ecotoxicity Values (Complete) data for DDT (157 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), experimental Koc values ranging from 1.13X10+5(2) to 3.5X10+5(3), indicate that DDT is expected to be immobile in soil(SRC). Volatilization of DDT from moist soil surfaces is not expected to be an important fate process(SRC) given a Henry's Law constant of 8.32X10-6 atm-cu m/mole(4). However, adsorption to soil is expected to attenuate volatilization(SRC). DDT is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 1.60X10-7 mm Hg at 20 °C(5). Reported half-lives for DDT in soils ranging from 2 years to > 15 years(6-9) indicate that DDT is expected to persist in aerobic terrestrial environments. Anaerobic conditions may be more amenable to biodegradation(10) with reported half-lives as low as 7 hours to 6.98 days in sediments and sludge(11,12).

AQUATIC FATE: Based on a classification scheme(1), experimental Koc values ranging from 1.13X10+5(2) to 3.5X10+5(3), indicates that DDT is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected to be an important fate process(4) based upon a Henry's Law constant of 8.32X10-6 atm-cu m/mole(5). Using this Henry's Law constant and an estimation method(4), volatilization half-lives for a model river and model lake are 8.5 and 68 days, respectively(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column(SRC). The estimated volatilization half-life from a model pond is 300 years if adsorption is considered(6). According to a classification scheme(7), BCF values ranging from 600 to 84,500(8,9), suggest bioconcentration in aquatic organisms is very high(SRC). Biodegradation of DDT in aquatic environments is variable with no observable degradation in marine waters(10), degradation rates of 67% after 24 weeks in sediments(11), and up to 95% conversion to DDD in river water samples(12).

AQUATIC FATE: There is ample evidence to demonstrate that DDT is very persistent in the environment. The dominant fate processes in aquatic environments are volatilization and sorption to biota and sediments, with the importance of sorption being determined by the amount of suspended particulate available in the water body. The ultimate transformation of DDT in the aquatic environment is probably by biotransformation, although one study indicates that indirect photolysis may also be a significant loss process for DDT in a natural water, with photolysis half-life on the order of a week. Photolysis of DDT in the gas phase has also been reported, but since DDT has been widely found throughout the biosphere, atmospheric transformations appear to be slow. There is also abundant evidence to demonstrate that bioaccumulation of DDT is an important process in the environment.

AQUATIC FATE: Direct photolysis of DDT in aqueous solution is very slow, with a half-life of probably greater than 150 years. Natural substances in some aquatic environments may cause indirect photolysis processes to be important for DDT transformation, with half-lives on the order of a few days or possibly ... hours for DDT loss. Half-lives for indirect photolysis of DDT are difficult to predict for general environmental assessments because of lack of information on the variability of natural waters to produce such indirect reactions through photosensitized, photo-initiated free radical, or other reactions.

For more Environmental Fate (Complete) data for DDT (6 total), please visit the HSDB record page.

DDT was detected in dairy milk (n = 65) and butter (n = 46) samples taken from Agra City, India at mean concns of 0.040 mg/L and 0.043 mg/kg, respectively(1). Fish and seafood collected at local harborside markets in Korea between 1997 and 2001 had a mean total DDT (o,p'-DDE, p,p-DDE, o,p'-DDD, p,p'-DDD, o,p'-DDT, and p,p'-DDT) concn of 3.84 ng/g wet wt, range 0.84 - 14.8 ng/g wet wt(2). DDT was detected in market fish collected from fisherman in four locations in Egypt in October 2001. The mean DDT concns were reported as follows (ng/g wet wt): no detection to 1.5 (South Sinai); no detection to 5.2 (Suez); no detection to 3.8 (Port Said); and 1.2 to 15.1 (Demietta)(3). DDT was detected in fresh vegetables from Nanjing, China sampled in June and October 2003 at mean concns (ng/g fresh wt) of: 14.8, carrot; 7.2, lettuce; 9.9, lettuce; 7.2, cabbage; 9.3, celery cabbage; 12.2, garlic leaf; 10.2, leek; 16.4, spinach; 10.8, tomato; and 12.3, pumpkin(4). A global assessment analyzing over 2 metric tons of farmed and wild salmon reported that there were noticeably higher concns of organochlorine contaminants (including DDT) in farmed salmon than in wild salmon. European-farmed salmon had higher contaminant loads than salmon raised in North or South America(5). A 5 year monitoring study analyzing agricultural products (domestic and imported) in the Hyogo Prefecture, Japan, detected DDT in 4 out of 291 samples of domestic garden radish at concns of <0.01 ug/g and <0.05 ug/g. Imported samples (4 out of 55) of broccoli pumpkin had concns of <0.01 ug/g and <0.05 ug/g(6).

During a study analyzing pesticide residues in major brands of infant formula in India, DDT was detected in 7 out of 10 sampled brands (manufactured between 2000 and 2001) at concns ranging from 0.6 ppb to 1.31 ppb(1). DDTs (sum of p,p'-DDD, p,p'-DDE, and p,p'-DDT) were detected in food items collected in Shanghai, China in August 2000 and April 2001. The reported concns are as follows (ng/g wt wt): 2.3 - 420, seafoods; 0.15 - 6.6, meats; <0.04, rice; 0.46, wheat; 0.40, apples; 0.83, grapes; <0.04 to 3.9, vegetables; 0.50 to 4.6, tea leaves; 6.0, mud snail; 4.2, crawfish; 1.9, milk (normal); 0.50, milk (process); 1.0, eggs(2). A global study of pesticide residues in butter was conducted between 1998 and 1999. Of the commercial butter samples from 22 countries, 20 countries had detectable levels of DDT. The mean concns were reported as follows (pg/g lipid): 120, Austria (n = 1); 780, Australia (n = 5); 590; 170, Canada (n = 6); 1180, Czech Republic (n = 1); 25230, India (n = 1); 1260, Israel (n = 1); 210, Japan (n = 1); 1360, Mexico (n = 3); 2290, Philippines (n = 2); 920, South Africa (n = 2); 700, Spain (n = 3); 270, Sweden (n = 3); 2730, Netherlands (n = 1); 1750, New Zealand (n = 1); 1250, Tunisia (n = 1); 130, United Kingdom (n = 2); 630, United States (n = 18)(3).

DDT was identified in the following food items during the FDA Total Diet Study. Highlights from the reported results are as follows: 0.0003 ppm, pan-cooked ground beef (n = 2); 0.0037 ppm, pan-cooked pork sausage (n = 12); 0.0002 ppm, boiled beef frankfurters (n = 1); 0.0004 ppm, white roll (n = 1); 0.0029 ppm, fresh/frozen boiled spinach (n = 26); 0.0010 ppm, raw celery (n = 13); 0.0009 ppm, raw radish (n = 11); 0.0017 ppm, baked white potato with skin (n = 17); 0.0009 ppm, potato chips (n = 4); 0.0021 ppm, plain milk chocolate candy bar (n = 20); 0.0009 ppm, fast food chicken nuggets (n = 1); 0.0032 ppm, dry roasted mixed nuts, no peanuts (n = 13); 0.0002 ppm, fast food quarter pound cheeseburger on bun (n = 1); 0.0020 ppm, olive/safflower oil (n = 1); 0.0050 ppm, baked fresh/frozen salmon steaks/filets (n = 1)(1).

During the period 1964-1969, DDT was detected in 9,158 out of 12,146 domestic meat products at an avg concn of 0.33 ppm, and in 3,082 out of 3,674 imported meat products at an avg concn of 0.41 ppm(1). During the period 1968-1969, DDT was detected in 3,383 out of 3,414 domestic samples of poultry at an avg concn of 0.15 ppm(1). During the period 1966-1969, DDT was detected in 251 out of 1,168 domestic grain samples at an avg concn of 0.02 ppm and in 6 out of 60 imported grains at trace concns (<0.005 ppm)(1). In a 1990 study of food products consumed in the US, DDT was identified, not quantified, in 154 out of 962 foods analyzed(2). An FDA monitoring study from 1978-1982 identified, DDT in 231 out of 1,050 food products in the US (3) and a similar FDA study from 1982-1986 identified DDT in 910 out of 3,792 foods analyzed(4). DDT was detected in tea from Belgium in 1991-1993 at max concns of 0.03-0.323 ppm(5). DDT was detected in meats consumed by the indigenous population of the Canadian Arctic at concns of 0.3-2.0 ng/g(6). It was also detected in raw blueberry and cranberry at concns of 0.1 and 1.0 ng/g, respectively(6).

For more Food Survey Values (Complete) data for DDT (6 total), please visit the HSDB record page.

The substance can be absorbed into the body by ingestion.

inhalation, skin absorption, ingestion, skin and/or eye contact

Oral (L85)

DDT was detected in 86 of 324 bovine milk samples taken from Punjab, India at mean concn of 0.01 mg/kg. 2.47% of the samples had concns above the allowable 0.05 mg/kg. The authors noted that DDT concns in milk has been declining since 1976(1). DDT was detected in 18% of sterilized cow's milk samples from Spain at a mean concn of 0.006 ppm and a range of 0.021 - 0.157 ppm(2). DDT was detected in cow's milk sampled from farms and bulk transporters in Veracruz, Mexico at a mean concn of 0.087 mg/kg fat basis (83.7% frequency). Total DDT (p,p'DDE, o,p'-DDT, p,p'-DDD, and p,p'-DDT) mean concn was 0.159 mg/kg fat basis(3).

DDT was detected in 3,312 of 12,989 samples at an avg concn of 30 ppb during the period of 1963-69 from the US(1); 501 of 4,638 whole milk samples from the US during the period 1969-76 at an avg concn of 6 ppb(2); 102 of 102 samples of human milk in 1979-1980 from the US at an avg concn of 0.19 ppm(3). DDT was detected in human milk fat samples from Mexico at concns of 0.24-1.98 ug/g(4). DDT was detected in human milk from Canada, Finland and the Netherlands at concns of 3.8-5.5 ppb(5), 1.2 ppb (avg)(6) and 0.1-3.3 ppb(7), respectively.

Based on more than 130 published values of DDT in human milk since 1951, the overall trend of DDT concn in milk declined throughout much of the world from 5,000 - 10,000 ug DDT/kg milk fat to around 1,000 ug DDT/kg milk fat today. The decline seems to correlate with the restriction of DDT use throughout the world. Levels can be high in areas still using DDT, even higher than the World Health Organization's recommended limit for infants(1).

DDT and metabolites were detected in the breast milk of 50 adult females in Mexico City. The mean values (lipid milk basis) were 0.162 ppm p,p'-DDT; 0.138 ppm o,p'-DDT; and 0.594 ppm 2,2(bis)p-chlorophyenyl-1-1-dichloroethylene (DDE).

... Biomagnification related to human exposures ... Reported for nursing infants /prior to 1965/. From analysis of DDT content of typical meals, it was est that lactating women had intake of 0.0005 mg/kg of DDT/day. Their milk contained 0.08 ppm ... This would result in infant dosage of 0.0112 mg/kg/day or approx 20 times as much as infants' mothers.

U061; As stipulated in 40 CFR 261.33, when DDT, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).

Cancelled, all products. Criteria of concern: Carcinogenicity, bioaccumulation, and hazard to wildlife and other chronic effects. (PR Notice 71-1 (1/15/71); 37 FR 13369 (7/7/72)).

As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive review of older pesticides to consider their health and environmental effects and make decisions about their continued use. Under this pesticide reregistration program, EPA examines newer health and safety data for pesticide active ingredients initially registered before November 1, 1984, and determines whether the use of the pesticide does not pose unreasonable risk in accordance to newer saftey standards, such as those described in the Food Quality Protection Act of 1996. Pesticides for which EPA had not issued Registration Standards prior to the effective date of FIFRA '88 were divided into three lists based upon their potential for human exposure and other factors, with List B containing pesticides of greater concern than those on List C, and with List C containing pesticides of greater concern than those on List D. DDT is found on List B. Case No: 2140; Case Status: No products containing the pesticide are actively registered ... The case /is characterized/ as "cancelled." Under FIFRA, pesticide producers may voluntarily cancel their registered products. EPA also may cancel pesticide registrations if registrants fail to pay required fees or make/meet certain reregistration commitments, or if EPA reaches findings of unreasonable adverse effects. Active ingredient (AI): dichlorodiphenyl trichloroethane; AI Status: The active ingredient is no longer contained in any registered pesticide products ... "cancelled."

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 1 lb or 0.454 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /DDT and metabolites/

p,p'-DDT is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.

(AZ) ARIZONA 0.10 ug/L

(FL) FLORIDA 0.1 ug/L

(ME) MAINE 1 ug/L

(MN) MINNESOTA 1 ug/L

(NH) NEW HAMPSHIRE 0.1 ug/L

P - Antiparasitic products, insecticides and repellents

QP - Antiparasitic products, insecticides and repellents

The temporal and dose-dependent hepatic estrogenicity of o,p'-DDT was investigated using complementary DNA microarrays in immature ovariectomized Sprague-Dawley rats with complementary histopathology and tissue-level analysis. Animals were gavaged with 300 mg/kg o,p'-DDT either once or once daily for 3 consecutive days. Liver samples were examined 2, 4, 8, 12, 18, or 24 h after a single dose or following three daily doses. For dose-response studies, a single dose of 3, 10, 30, 100, or 300 mg/kg body weight o,p'-DTT was administered for 3 consecutive days. Genes associated with drug metabolism (Cyp2b2 and Cyp3a2), the nuclear receptors constitutive androstane receptor (CAR) and pregnane X receptor (PXR), cell proliferation (Ccnd1, Ccnb1, Ccnb2, and Stmn1), and oxidative stress (Gclm and Hmox1) were significantly induced. Cyp2b2 exhibited dose-dependent regulation and was significantly induced across all time points, while cell proliferation- and oxidative stress-related genes exhibited transient induction. The induction of Cyp2b2 and Cyp3a2 mRNA levels suggest PXR/CAR activation, consistent with expression of genes associated with oxidative stress. Few genes known to be estrogen receptor (ER) regulated were differentially expressed when compared to the hepatic gene expression profile elicited by ethynyl estradiol in immature ovariectomized C57BL/6 mice using the same study design and analysis methods. These data indicate that o,p'-DDT elicits PXR/CAR-, not ER-, mediated gene expression in the rat liver. Based on the species-specific differences in CAR regulation, the extrapolation of rodent DDT hepatocarcinogenicity to humans warrants further investigation.

Stability of cell-to-cell interactions and integrity of junctional membrane proteins are essential for biological processes including cancer prevention. The present study shows that DDT, a non-genomic carcinogen used at a non-cytotoxic dose (1 uM), rapidly disrupted the cell-cell contacts and concomitantly induced the formation of cytoplasmic vacuoles close to the plasma membrane in the SerW3 Sertoli cell line. High-resolution deconvolution microscopy reveals that this vacuolization process was clathrin-dependent since a hyperosmotic media (0.2 M sucrose) blocked rhodamine-dextran endocytosis. In response to DDT, junctional proteins such as Cx43, N-Cadherin and ZO-1 were internalized and present in vacuoles. In Cx43-GFP transfected cells, time lapse videomicroscopy demonstrates that DDT rapidly enhanced fragmentation of the gap junction plaques and abolished the gap junction coupling without major modification of Cx43 phosphorylation status. Repeated exposure to DDT resulted in chronic gap junction coupling injury. The present results demonstrate that one of the early effects of DDT is to interfere with the plasma membrane and to perturb its function, specifically its ability to establish cell-cell junctions that are essential for tissue homeostasis and control of cell proliferation and differentiation. Such an alteration may play a specific role during carcinogenesis.

/DDT/ is capable of altering transport of sodium and potassium ions across axonal membranes, resulting in increased negative afterpotential, prolonged action potentials, repetitive firing after single stimulus, and spontaneous trains of action potentials. Specifically, DDT seems to inhibit inactivation of sodium channels and the activation of potassium conductance.

DDT, at concentrations known to inhibit cell-cell communication, increased cellular (45)calcium uptake and inhibited its efflux in Chinese Hamster V-79 fibroblast cell line. It inhibited Ca, Mg-activated ATPase of plasma membrane. Hypothesis was proposed that increase in intracellular concentration of calcium results in closure of central opening of the gap junction causing cessation of gap junction-mediated intercellular communication.

For more Mechanism of Action (Complete) data for DDT (10 total), please visit the HSDB record page.

1-2 years to eliminate absorbed dose; [TDR, p. 440]

Highly lipophilic pesticides, such as DDT and leptophos, are /eliminated/ at extremely slow rates, with half life of about 300 minutes in the rat.

Female rats were dosed orally with (14)C-ring-labeled p,p'-DDT during pregnancy or lactation. Clearance of DDT in milk decreased with a rate constant of -0.096 & half life of 7.2 days. DDD & DDE increased in neonate liver as DDT decreased. Avg half life was 10.6 hr in tissues & fetus.

When technical DDT was added to rations of sheep (250 ppm p,p'-DDT), a plateau at 524 ppm p,p'-DDT, 75 ppm p,p'-DDD & 25 ppm p,p'-DDE in subcutaneous fat was reached in 8 weeks. The computed depletion half life was 90, 26, & 223 days, respectively.

Atlantic salmon (Salmo salar) fry were injected im with tritiated p,p'-DDT. About 60% of the material remained after 8 weeks. DDT conversion to DDE exhibited a half life of 60 days.

For more Biological Half-Life (Complete) data for DDT (7 total), please visit the HSDB record page.

The metabolism of p,p'-DDT has been extensively examined in the rat, and approximately nine metabolites have been identified. In humans, the degradation of DDT proceeds by dehydrochlorination to the unsaturated pp'-DDE [1,1-dichloro-2,2-bis (p-chlorophenyl)ethylene] and/or by substitution of a hydrogen for one ethyl binding chlorine atom yielding pp'-DDD [1,1-dichloro-2,2-bis (p-chlorophenyl)ethane]. DDD is further metabolized through a series of intermediates yielding the carboxy acid form, p,p'-DDA [2,2-bis(p- chlorophenyl)acetic acid]. DDA is relatively water soluble and is excreted primarily in the urine (30). ... Ingestion of DDT and DDT metabolites in six volunteers given technical DDT (5, 10, 20 mg/day) or pp'-DDE, p,p'-DDD, or p,p'-DDA (5 mg/day for 21 to 183 days), demonstrating that within 24 hr of ingestion of DDT, urinary DDA excretion increased. ... Excretion of DDT as DDA appeared to depend totally on the preferential reductive dechlorination of DDT to DDD (rather than DDE), and thence to DDA.

Metabolic fate ... studied in hamsters ... in view of hamster's tolerance to acute doses that were lethal to mouse, and of its insensitivity to long-term dietary dosages that induce hepatic tumors in mouse. ... Comparative studies ... of sub-acute dosages of p,p'-DDT in Syrian Golden hamster and Swiss mouse ... revealed that both species excreted the glucuronide of p,p'- bis(p-chlorophenyl)-acetic acid as major urinary metabolite, but that mouse alone excreted p,p'-DDE in urine. Feces of both ... contained p,p-'DDD and p,p'-DDT. In view of absence of p,p'-DDE ... in hamster, and its only modest accumulation in liver (compared with that in mouse liver), this metabolite has been incriminated as ultimate liver tumorigen in mouse.

... Bis(p-chlorophenyl)-methane (DDM) and bis(p-chlorophenyl)-methylketone (DBP) in chicken eggs and young chicks /have been identified as metabolites of DDT resulting from bis(p-chlorophenyl)-acetic acid/. Not only was DBP found to result from ... Bis(p-chlorophenyl)-acetic acid with DDM as intermediate, but DBP was only metabolite of DDE administration directly to eggs of chicks.

Housefly ... converted DDT to DDE and unidentified water sol products possibly conjugated with carbohydrate. Fly homogenates, in presence of NADPH2, converted DDT to kelthane.

For more Metabolism/Metabolites (Complete) data for DDT (22 total), please visit the HSDB record page.

DDT is absorbed in the stomach and intestine, after which it enters the lymphatic system and is carried throughout the body and incorporated into fatty tissues. Metabolism of DDT occurs mainly via cytochrome P-450 enzymes in the liver and kidney, where it undergoes reductive dechlorination to DDD (dichlorodiphenyldichloroethane) and DDE (dichlorodiphenyldichloroethylene). These compounds are further degraded into additional metabolites, mainly DDA (bis(p-chlorophenyl) acetic acid), which are excreted in the urine. (L85)

It is readily absorbed when dissolved in oils, fats, or lipid solvents but is poorly absorbed as dry powder or aqueous suspension. Once absorbed, DDT concentrates in adipose tissue. Storage ... in fat is protective, because it decreases amount of chemical at its site of toxic action, the brain. ... At constant rate of intake, concentration ... in adipose tissue reaches steady-state value and remains relatively constant. ... When exposure ceases, DDT is eliminated ... slowly. Elimination ... Estimated to be at rate of approx 1% of stored DDT excreted/day.

Most DDT dust is of such large particle size that any that is inhaled is deposited in upper respiratory tract and eventually ... swallowed. ... Dermal absorption is very limited.

... Fecal excretion of DDT metabolites ... in rat ... exceeded urinary excretion irrespective of route of administration. ... Excretion ... in milk has been reported ... .

... Placental passage of DDT in dogs has been demonstrated and these findings have been confirmed in mice by whole-animal autoradiography. In fetuses ... shown to be localized in liver, adipose tissue and intestine.

For more Absorption, Distribution and Excretion (Complete) data for DDT (21 total), please visit the HSDB record page.

Formerly used as an insecticide and pesticide; [HSDB]

All agricultural uses cancelled in 1972 by EPA; [Sullivan, p. 660]

Farming (Pesticides) [Category: Industry]

For DDT (USEPA/OPP Pesticide Code: 029201) there are 0 labels match. /SRP: Not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

The active ingredient is no longer contained in any registered pesticide products ... "cancelled" /in the USA/.

DDT may be produced and used only for disease vector control and according to the recommendations and guidelines of the World Health Organization. DDT will be used when safe, effective and affordable alternatives are not locally available in a country. The World Health Organization recommends only indoor residual spraying (spraying only on the inside walls of buildings) of DDT for disease vector control.

... the condensation of chlorobenzene with trichloroacetaldehyde ... reaction ... /produces/ p,p'-DDT ... technical product ... that contains up to 30% of o,p'-DDT ... which, being of insecticidal value, is not usually removed.

DDT refers to technical /grade/ DDT, which is usually composed of: 77.1% p,p'-DDT, 14.9% o,p'-DDT, 0.3% p,p'-DDD, 0.1% o,p'-DDD, 4.0% p,p'-DDE, 0.1% o,p'-DDE, and 3.5% unidentified compounds.

(1971) 90% /of us production was/ exported

(1972) 1.61X10+10 g

(1975) 2.15X10+10 g (incl formulations)

(1978) 1.37X10+10 g

For more U.S. Exports (Complete) data for DDT (8 total), please visit the HSDB record page.

(1972) 2.27X10+10 G

(1975) 4.3X10+10 G (EST, INCL FORMULATIONS)

(1983) not produced commercially in US

Essentially 100% as an insecticide

90% exported (1971); 9% on cotton, 1% on a variety of vegetables, field crops, and livestock (primarily cattle); since 1972, virtually all DDT produced in the US has been exported; less than 450 million grams was consumed in the US for emergency use (1974)

Condensing chloral or chloral hydrate with chlorobenzene in presence of sulfuric acid.

Chlorobenzene undergoes acid-catalyzed condensation with trichloroacetaldehyde to produce DDT.

Preparation: ... P. Muller, US 2329074 (1944 to Geigy).

Grade: Technical, purified, aerosol, USP, as chlorophenothane

... /Medical prepn is/ mixture of 10% DDT powder with talc or any other suitable diluent.

Dicophane Application: Applic Dicophan; DDT Application. Dicophane 2 g, emulsifying wax 4 g, xylene of commerce 15 ml, citronella oil 0.5 ml, water to 100 ml.

Dicophane Dusting-powder: Conspersus Dicophani; DDT Dusting-powder. Dicophane 10 g, calcium carbonate 10 g, and sterilized light kaolin or light kaolin (natural) 80 g.

For more Formulations/Preparations (Complete) data for DDT (92 total), please visit the HSDB record page.

Food Contaminant -> CONTAMINANT -> JECFA Functional Classes

INSECTICIDES

Benzene, 1,1'-(2,2,2-trichloroethylidene)bis[4-chloro-: ACTIVE

The WHO Recommended Classification of Pesticides by Hazard identifies DDT (technical grade) as Class II: moderately hazardous; Main Use: insecticide. According to the PIC /Prior Informed Consent/ Convention, export of /DDT/ can only take place with the prior informed consent of the importing Party. ...(further information can be found at: http://www.pic.int/). The use and production of ... DDT ... is prohibited or severely restricted by the Stockholm convention on persistent organic pollutants, which entered force on 17 May 2004. See http://www.pops.int/.

... Released for commercial use in USA on August 31, 1945; 1946 was 1st full yr of use. At that time, DDT was introduced in malaria-stricken regions of the world and remains ... one of primary insecticides for control of malaria through eradication of vectors. From 1946-1972, DDT was one of most widely used agric insecticides in USA and other countries.

Insect resistance to DDT has become widespread in many species. This has been shown to be attributable to selection of naturally occurring genotypes that possess enhanced amt of enzyme DDT-ase ... which detoxifies DDT to inactive DDE.

DDT ... was patented as insecticide in 1939 by Swiss chemist, Paul Muller.

For more General Manufacturing Information (Complete) data for DDT (11 total), please visit the HSDB record page.